In humans, there is a locus on chromosome 22 that encodes 7 APOEBC3 genes encoding APOBEC3A (A3), A3B, A3C, A3DE, A3F, A3G and A3H. To distinguish them from those in other animals they are generally abbreviated to hA3A, hA3B, hA3C, hA3DE, hA3F, hA3G and hA3H. While there is still much work to do defining substrate specificity for the ensemble of these enzymes, it is clear that all seven are capable of deaminating cytidine residues in single stranded DNA.
Some of these APOBEC3 deaminases have been demonstrated to have anti-retroviral effects (Lecossier et al., 2003, Mangeat et al., 2003, Mariani et al., 2003, Suspene et al., 2004, Zhang et al., 2003). Human immunodeficiency virus type (HIV-1) cDNA in particularly is vulnerable to the action of the cytoplasmic hA3F and hA3G cytidine deaminases (hA3F & hA3G) (Harris et al., 2003, Wiegang et al., 2004). By contrast hA3A, hA3C and hA3H are mainly nuclear while hA3B is both nuclear and cytoplasmic (Bogerd et al., 2006, Kinomoto et al., 2007).
Human A3A and hA3B are expressed in psoriatic keratinocytes and hA3A is up-regulated in acne lesions and can be induced by phorbol-12-myristate 13-acetate (Madsen et al., 1999, Trivedi et al., 2006). Interestingly, hA3H is also expressed in normal skin (Dang et al., 2006, OhAinle et al., 2006).